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DNBS-induced colonic damage was improved in passive-cigarette-smoking rats. This was accompanied by attenuation of the elevated colonic myeloperoxidase and inducible nitric oxide synthase activities and leukotriene B4 level. Likewise, the augmentation in colonic levels of TNF-alpha, interleukin (IL)-1 beta, and IL-6 in colitis rats was also alleviated by passive cigarette smoking. In contrast, the deprivation of colonic IL-10 during colitis was preserved in cigarette-smoking rats. These effects were similarly accomplished by pentoxifylline and, to some degree, by cyclosporin A.
Animal laboratory of a university hospital.
PTX may be an anti-fibrosis agent capable of inhibiting renal fibrosis in a rat model of crescentic glomerulonephritis. Blockade of TGF-beta1 expression and Smad2/3 activation may be a mechanism by which PTX inhibits renal fibrosis.
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1. Disseminated intravascular coagulation frequently accompanies Gram-negative sepsis and may contribute to widespread deposition of microthrombi. Besides the endotoxin-induced activation of coagulation, an important role for the fibrinolytic system has been postulated. The precise mechanisms underlying these fibrinolytic changes during endotoxaemia are not known but have been suggested to be mediated directly by cytokines or secondary to thrombin generation. 2. In the present study we have delineated in detail the fibrinolytic response to a bolus injection of endotoxin in non-human primates and analysed the contribution of cytokines and thrombin generation to the endotoxin-induced release of tissue-type plasminogen activator and plasminogen activator inhibitor 1. Chimpanzees received a bolus injection of endotoxin alone or in combination with blocking monoclonal antibodies directed against tumour necrosis factor or interleukin 6 or in combination with pentoxifylline. Furthermore, to assess the effect of coagulation activation on the activation of fibrinolysis, another group of chimpanzees received endotoxin in combination with either anti-tissue factor antibodies or recombinant hirudin. 3. Infusion of endotoxin induced a rapid increase in plasminogen activator activity and tissue-type plasminogen activator antigen levels and subsequent plasmin generation, reaching peak levels 2h after endotoxin administration. Plasminogen activator inhibitor 1 levels remained constant for the first 2 h, after which time a steep increase was observed. Plasminogen activator activity and plasmin generation decreased simultaneously with the rise in plasminogen activator inhibitor 1 levels. Fibrinolytic activity remained suppressed during the remainder of the study owing to sustained increased levels of plasminogen activator inhibitor 1. The administration of pentoxifylline strongly attenuated the release of tissue-type plasminogen activator and plasminogen activator inhibitor 1, whereas the antitumour necrosis factor antibodies blocked the fibrinolytic response entirely. In contrast, interleukin 6-neutralizing antibodies did not affect the fibrinolytic response. Although endotoxin-induced generation of thrombin was completely prevented by the administration of tissue factor-neutralizing antibodies or by hirudin, no effect on the fibrinolytic response was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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Complete healing of the reference ulcer occurred in 23 of the 38 patients treated with oxpentifylline and in 12 of the 42 patients treated with a placebo. Life table analysis showed that the proportion of ulcers healed at six months was 64% in the group treated with oxpentifylline compared with 34% in the group treated with a placebo (log rank test chi 2 = 4.78, p = 0.03), which was significant (odds ratio = 1.81, 95% confidence interval 1.20 to 2.71).
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To investigate whether pentoxifylline (PTX) could influence the increased cytokine gene expression in the retina flowing transient ischemia, and if so, whether it acts through the modulation of nuclear factor kappa B (NF-kappaB) activation.
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Pentoxifylline pretreatment protects rat gastric mucosa against indomethacin-induced damage. Lipid peroxidation after indomethacin treatment (determined as thiobarbituric acid reactants) was significantly reduced by a single dose of pentoxifylline. The same was true for pentoxifylline administration for 6 days. There is a relationship between reduced lipid peroxidation, decreased number of circulating activated neutrophils and diminished disposition for acute gastric mucosal lesions induced by indomethacin in pentoxifylline-pretreated rats.
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The effects of pentoxifylline and progesterone on human sperm capacitation and acrosomal exocytosis were investigated using chlortetracycline (CTC) fluorescence. Continuous exposure to 3.60 mM pentoxifylline caused significant changes in distribution of the three CTC patterns (F, B and AR) compared with control suspensions. Initially, the main effect was promotion of the F to B transition, followed by increases in acrosome-reacted (AR) pattern cells as well. Such responses would be consistent with a pentoxifylline-mediated inhibition of cAMP phosphodiesterase leading to increased availability of cAMP. When continuous and short-term exposure to pentoxifylline were compared, very similar responses were observed: both pentoxifylline-treated groups had significantly more capacitated cells (B and AR patterns) than controls. Progesterone tested at 1, 10 and 100 micrograms ml-1 elicited a similar response to that observed with pentoxifylline, with both capacitation and acrosomal exocytosis being stimulated. Cells incubated in 2 x Ca2+ (3.6 mM) medium were even more responsive to progesterone treatment than those in standard 1 x Ca2+ (1.8 mM) medium, with a threefold decrease in cells exhibiting the F pattern (characteristic of uncapacitated, acrosome-intact cells) and a marked increase in AR cells. These responses are consistent with a progesterone-mediated rise in intracellular Ca2+ that could promote completion of capacitation and initiation of acrosomal exocytosis. Used in combination, pentoxifylline followed by progesterone treatment produced significantly more AR pattern cells than either compound individually.(ABSTRACT TRUNCATED AT 250 WORDS)
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There is little evidence of benefit from using corticosteroids or intravenous immunoglobulins to reduce the risk of heart valve lesions in patients with acute rheumatic fever. The antiquity of most of the trials restricted adequate statistical analysis of the data and acceptable assessment of clinical outcomes by current standards. Additionally there was substantial risk of bias, so results should be viewed with caution. New randomised controlled trials in patients with acute rheumatic fever to assess the effects of corticosteroids such as oral prednisone and intravenous methylprednisolone, and other new anti-inflammatory agents are warranted. Advances in echocardiography will allow for more objective and precise assessments of cardiac outcomes.
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Cerebral malaria is the most common cause of non-traumatic encephalopathy in the world. The mainstay of therapy is either quinine or artemisinin, both of which are effective antimalarials. The clinical picture of cerebral malaria may persist or even become worse in spite of the clearance of parasites from blood. The death rate is unacceptably high even with effective antimalarials in tertiary care hospitals. The mortality increases in presence of multi organ failure (renal failure, jaundice, respiratory distress, severe anaemia, lactic acidosis, etc.). The pathogenesis of cerebral malaria is multifactorial and includes clogging, sequestration, rosette formation, release of cytokines, cerebral oedema, increased intracranial hypertension, etc. Attempts are made to use adjuvant therapy which will act through alternate mechanisms and address one or more of the pathogenetic processes. In this review, we have discussed the role of corticosteroids, pentoxifylline, desferrioxamine, mannitol and newer agents in the treatment of cerebral malaria. Though the literature on adjuvant therapy in cerebral malaria is large enough, there are a number of shortcomings in the clinical trials, many being open and non randomized or of very small sample size. Further research is of utmost importance through large multicentric, double-blind controlled trials to show the efficacy of any of these drugs.
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Twenty four patients fulfilling the criteria of septic shock were included in this study. Twelve patients received PTX (therapy group) and 12 patients matched for diagnosis, age and gender served as the control group.
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This article updates the June 2014 Living FRISBEE (Living FRISBEE: Living FRIendly Summary of the Body of Evidence using Epistemonikos). It incorporates a new systematic review identifying one study not included in previous reviews. The new evidence leads to substantial changes in the existing evidence.
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Inflammation plays a pivotal role in the pathogenesis of organ dysfunction after cardiopulmonary bypass (CPB). The aim of this study was to investigate whether pentoxifylline (PTX) has effects on the inflammatory process and leukocytes in cardiac surgery patients undergoing CPB.
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We demonstrated that midbrain astrocytes play an important role in the development of analgesic tolerance to morphine.
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Intestinal ischemia/reperfusion (I/R) causes local and remote injuries that are multifactorial and essentially inflammatory in nature. To study the putative influences of nitric oxide (NO) and tumor necrosis factor alpha (TNF-alpha) on the release of interleukin (IL) 1beta and IL-10 and the involvement of lymphatic system on a systemic inflammation caused by I/R, we have quantified the serum and lymph levels of IL-1beta and IL-10 in rats during I/R after treatment with inhibitors of NO synthase (N-nitro-L-arginine methyl ester hydrochloride [L-NAME]) or TNF-alpha (pentoxifylline [PTX]). Intestinal I/R was performed by means of a 45-min occlusion of the mesenteric artery, followed by 2-h reperfusion; groups of rats subjected to I/R had the thoracic lymph duct ligated immediately before the procedure. The I/R caused a significant increase of the serum levels of IL-1beta and IL-10 in rats with intact thoracic lymph duct, whereas the thoracic duct ligation blunted the serum release of IL-1beta and elevated that of IL-10. The levels of the cytokines collected in the lymph after I/R increased, and even more increase was observed in L-NAME-treated rats. L-NAME significantly increased the lymph levels of IL-1beta and IL-10; in serum, however, only IL-1beta increased in rats with either intact or ligated thoracic lymph duct. The treatment with PTX reduced the serum levels of IL-1beta irrespective of the lymph circulation interruption but was effective to increase the IL-10 levels in intact rats during I/R. The lymphatic levels of IL-1beta of rats subjected to I/R were reduced and those of IL-10 were increased after treatment with PTX. In conclusion, during I/R, the serum levels of IL-1beta seem modulated by stimulant mechanisms that could be associated with TNF-alpha and inhibited by NO and by the integrity of the thoracic lymphatic flow. On the other hand, IL-10 seems controlled by TNF-alpha-related, largely NO-independent mechanisms. Thus, it is reasonable to suppose that an endogenous mechanism that can limit the systemic inflammatory response ensuing an I/R splanchnic trauma exists.
The fetus and the neonate are particularly vulnerable to injury caused directly by immunologic mechanisms or inflicted by infectious agents that take advantage of their relatively immature and inexperienced immune system. With increasing survival of high-risk neonates in the surfactant era, prevention/treatment of sepsis and chronic lung disease (CLD) has emerged as an area of priority in neonatal research. Considering the role of inflammatory mediators in the pathogenesis of sepsis and CLD, the clinical application of immunomodulator therapy to neonatology is perhaps more important at present than ever. Advances in molecular biology and immunology have led to development of newer immune modulator therapies that are directed towards specific cells or cytokines rather than resulting in a general suppression of the immune response. Failure of promising, newer immunomodulator therapies in sepsis trials in adults has, however, clearly documented the difficulties in diagnosing/correcting the imbalance between pro- and anti-inflammatory responses. As in the case of sepsis, development of a single magic bullet for prevention/management of a multi-factorial illness like CLD may be difficult, as prevention of prematurity - the single most important high-risk factor for CLD - is an unachievable goal at present. As new frontiers are being explored, older, well-established therapies like antenatal anti-D immunoglobulin prophylaxis continue to emphasize the tremendous potential of immunomodulator therapy in neonatology/perinatology. The current immunomodulators/immunotherapeutic agents with established/potential clinical applications in the perinatal period are reviewed.
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In this randomized controlled trial, 32 patients with extensive psoriasis were divided into four groups: group A received sulfasalazine; group B received pentoxifylline; group C received both drugs; and group D received methotrexate. The Psoriasis Area and Severity Index (PASI) score was done at weeks 0, 2, 4, 6 and 8.
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Tumour necrosis factor-alpha is thought to be important in the pathogenesis of portal hypertension. Oxpentifylline (pentoxifylline) and thalidomide inhibit endotoxin-induced tumour necrosis factor-alpha production in vitro.
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1. The effects of caffeine and related compounds on responses mediated by inhibitory amino acids were investigated in freshly dissociated rat hippocampal pyramidal neurones by conventional and nystatin perforated patch-clamp techniques. 2. Glycine and gamma-aminobutyric acid (GABA) evoked Cl- currents in hippocampal neurones. The half-maximum effective concentrations (EC50) of glycine and GABA were 8.5 x 10(-5) and 5 x 10(-6) M, respectively. 3. Caffeine reversibly inhibited both 10(-4) M glycine- and 10(-5) M GABA-induced Cl-currents in a concentration-dependent manner. The half-maximum inhibitory concentrations (IC50) of caffeine were 4.5 x 10(-4) M for the glycine response and 3.6 x 10(-3) M for the GABA response. 4. Caffeine shifted the concentration-response curve of IGly to the right without affecting the maximum response. 5. The inhibitory action of caffeine did not show voltage-dependency. 6. The blocking action of caffeine was not affected by intracellular perfusion with 5 mM BAPTA or by pretreatment with the protein kinase A inhibitor, H-8. This excludes the participation of Ca2+ or cyclic AMP in the inhibitory action of caffeine. 7. Caffeine failed to inhibit the augmentations of aspartate- and N-methyl-D-aspartate (NMDA) -gated current by glycine, suggesting that caffeine has no effect on the allosteric glycine binding site on the NMDA receptor. 8. The inhibitory effects of some xanthine derivatives on IGly were compared. The inhibitory potency of those compounds on IGly was in the order of pentoxifylline > theophylline > or = caffeine > paraxanthine > IBMX > or = theobromine > dyphylline. Xanthine had no effect. 9. The results indicate that methylxanthines including caffeine may act directly on the glycine receptor Cl- channel complex in rat hippocampal pyramidal neurones. The blockade of the inhibitory amino acid response by methylxanthines may be involved in the excitatory side effects of methylxanthines in the mammalian central nervous system.
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This review of recent articles on ocular toxicology concentrates on undesirable effects on the eye induced by systemically used xenobiotics. These effects include the corticosteroid-induced glaucoma and cataracts (especially in children), chloroquine-induced heart block and retinopathy, its possible protection by platelet aggregating factor antagonists, oculopathy after intracarotid chemotherapy with nitrosyl-urea or cisplatin, ketoconazole-induced papilledema, cytarabine-induced photophobia, ethambutol HCl-induced visual deficits, psychotherapeutic-agent overdose-induced ocular bobbing, amiodarone-induced cataracts, and imipramine HCl-induced angle-closure glaucoma. Also reviewed are the role of hormone levels in diabetic retinopathy, the therapeutic use of clonidine for perioperative intraocular pressure spikes, the increase in ocular blood flow by pentoxifylline, and decrease by nicotine, the potential for the reduction in drop size of mydriatic medications, a theory for sulfonamide-induced myopia, and guidelines for animal models of ocular toxicity. No drug achieves ultimate efficacy or ultimate safety. Thus, the decision to employ a given therapy involves a physician's evaluation of its therapeutic index, the ratio between efficacy and toxicity.
Behçet's disease is a chronic relapsing vasculitis characterized by recurrent aphthous oral and genital ulcerations with uveitis. Multiple organs can be involved. Entero-Behçet's disease is often uncontrollable, relapsing, and can cause acute intestinal bleeding or perforation. We utilized a combination therapy including 600 mg of pentoxifylline per day, in two doses, to treat three female patients and observed the subsequent changes in clinical symptoms, serum C reactive protein levels, and endoscopic findings. In all three patients, clinical symptoms as well as serum C reactive protein levels improved immediately. Endoscopically, lower intestinal lesions were significantly reduced or healed in all of them. Combination therapy including pentoxifylline appears to be clinically effective in the patients with entero-Behçet's disease.
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Genotyping was undertaken in 898 cases with severe alcoholic hepatitis, recruited through the UK Steroids or Pentoxifylline for Alcoholic Hepatitis (STOPAH) trial, and 1188 White British/Irish alcohol dependent controls with no liver injury, recruited via University College London. Subsequent drinking behaviour was classified, in cases surviving ≥90days, as abstinent or drinking. The relationship between rs738409 genotype, drinking behaviour and survival was explored.
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To assess the physiological role of intracellular Ca(2+) in the changes of microrheological red blood cell (RBC) properties (RBC deformability and aggregation), we employed several types of chemicals that can increase and decrease of the intracellular Ca(2+) concentration. The rise of Ca(2+) influx, stimulated by mechanical loading, A23187, thrombin, prostaglandin F(2α) was accompanied by a moderate red cell deformability lowering and an increase of their aggregation. In contrast, Ca(2+) entry blocking into the red cells by verapamil led to a significant RBC aggregation decrease and deformability rise. Similar microrheological changes were observed in the red blood cells treated with phosphodiesterase inhibitors IBMX, vinpocetine, rolipram, pentoxifylline. When forskolin (10 μM), an AC stimulator was added to RBC suspension, the RBC deformability was increased (p <0.05). Somewhat more significant deformability rise appeared after RBC incubation with dB-AMP. Red cell aggregation was significantly decreased under these conditions (p<0.01). On the whole the total data clearly show that the red cell aggregation and deformation changes were connected with an activation of both intracellular signaling pathways: Ca(2+) regulatory mechanism and Gs-protein/adenylyl-cyclase-cAMP system. And the final red cell microrheological regulatory effect is connected with the crosstalk between these systems.
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To evaluate the effect of hypervolemic hemodilution on cerebral blood flow (CBF) two protocols have been performed: A) Ten randomly selected baboons have been treated with either low molecular dextrane (10 ml/kg) or normal saline (10 ml/kg). Regional cerebral ischemia was produced in all baboons. CBF increased selectively in the ischemic territory but not in the normally perfused tissue. B) Forty patients with acute cerebral ischemia were treated on day onset of symptoms with either dextrose, low molecular weight dextrane, hydroxyethyl starch or pentoxifylline. After intravenous infusion of the substances CBF increased only in the groups treated with dextrane- or starch-solution. Ischemic tissue benefitted more from hypervolemic hemodilution than normally perfused tissue. It was concluded that hypervolemic hemodilution leads to increase of cerebral blood flow, more in ischemic than in normally perfused brain tissue.